Are Sphingolipids and Serine Dipeptide Lipids Underestimated Virulence Factors of Porphyromonas gingivalis?

The keystone periodontal pathogen produces phosphorylated dihydroceramide lipids (sphingolipids) such as phosphoethanolamine dihydroceramide (PE DHC) and phosphoglycerol dihydroceramide (PG DHC) lipids. Phosphorylated DHCs (PDHCs) from can affect a number of mammalian cellular functions, such as pot...

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Veröffentlicht in:Infection and immunity 2018-07, Vol.86 (7)
Hauptverfasser: Olsen, Ingar, Nichols, Frank C
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description The keystone periodontal pathogen produces phosphorylated dihydroceramide lipids (sphingolipids) such as phosphoethanolamine dihydroceramide (PE DHC) and phosphoglycerol dihydroceramide (PG DHC) lipids. Phosphorylated DHCs (PDHCs) from can affect a number of mammalian cellular functions, such as potentiation of prostaglandin secretion from gingival fibroblasts, promotion of RANKL-induced osteoclastogenesis, promotion of apoptosis, and enhancement of autoimmunity. In , these lipids affect anchoring of surface polysaccharides, resistance to oxidative stress, and presentation of surface polysaccharides (anionic polysaccharides and K-antigen capsule). In addition to phosphorylated dihydroceramide lipids, serine dipeptide lipids of are implicated in alveolar bone loss in chronic periodontitis through interference with osteoblast differentiation and function and promotion of osteoclast activity. As a prerequisite for designation as bacterial virulence factors, bacterial sphingolipids and serine dipeptide lipids are recovered in gingival/periodontal tissues, tooth calculus, human blood, vascular tissues, and brain. In addition to , other bacteria of the genera , , , , and produce sphingolipids and serine dipeptide lipids. The contribution of PDHCs and serine dipeptide lipids to the pathogenesis of periodontal and extraoral diseases may be an underappreciated area in microbe-host interaction and should be more intensively investigated.
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Phosphorylated DHCs (PDHCs) from can affect a number of mammalian cellular functions, such as potentiation of prostaglandin secretion from gingival fibroblasts, promotion of RANKL-induced osteoclastogenesis, promotion of apoptosis, and enhancement of autoimmunity. In , these lipids affect anchoring of surface polysaccharides, resistance to oxidative stress, and presentation of surface polysaccharides (anionic polysaccharides and K-antigen capsule). In addition to phosphorylated dihydroceramide lipids, serine dipeptide lipids of are implicated in alveolar bone loss in chronic periodontitis through interference with osteoblast differentiation and function and promotion of osteoclast activity. As a prerequisite for designation as bacterial virulence factors, bacterial sphingolipids and serine dipeptide lipids are recovered in gingival/periodontal tissues, tooth calculus, human blood, vascular tissues, and brain. In addition to , other bacteria of the genera , , , , and produce sphingolipids and serine dipeptide lipids. 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Phosphorylated DHCs (PDHCs) from can affect a number of mammalian cellular functions, such as potentiation of prostaglandin secretion from gingival fibroblasts, promotion of RANKL-induced osteoclastogenesis, promotion of apoptosis, and enhancement of autoimmunity. In , these lipids affect anchoring of surface polysaccharides, resistance to oxidative stress, and presentation of surface polysaccharides (anionic polysaccharides and K-antigen capsule). In addition to phosphorylated dihydroceramide lipids, serine dipeptide lipids of are implicated in alveolar bone loss in chronic periodontitis through interference with osteoblast differentiation and function and promotion of osteoclast activity. As a prerequisite for designation as bacterial virulence factors, bacterial sphingolipids and serine dipeptide lipids are recovered in gingival/periodontal tissues, tooth calculus, human blood, vascular tissues, and brain. In addition to , other bacteria of the genera , , , , and produce sphingolipids and serine dipeptide lipids. The contribution of PDHCs and serine dipeptide lipids to the pathogenesis of periodontal and extraoral diseases may be an underappreciated area in microbe-host interaction and should be more intensively investigated.</description><subject>Alveolar Bone Loss - etiology</subject><subject>Ceramides - chemistry</subject><subject>Ceramides - physiology</subject><subject>Chronic Periodontitis - etiology</subject><subject>Humans</subject><subject>Lipopeptides - chemistry</subject><subject>Lipopeptides - physiology</subject><subject>Minireview</subject><subject>Osteoclasts - physiology</subject><subject>Phosphorylation</subject><subject>Porphyromonas gingivalis - pathogenicity</subject><subject>Toll-Like Receptor 2 - physiology</subject><subject>Virulence Factors - chemistry</subject><subject>Virulence Factors - physiology</subject><issn>0019-9567</issn><issn>1098-5522</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>3HK</sourceid><recordid>eNpVkc1vEzEQxS1ERUPhxhl87IEt_rb3AopaSiNFAqmUq2WvZxPDxl7sTaX-92xJW8FpNJqn37yZh9AbSs4oZeZDdPGMEMJlQ80ztKCkNY2UjD1HC0Jo27RS6WP0stafcyuEMC_QMWsVZ0yYBfq1LICvx21MmzzEMYaKXQr4GkpMgC_iCOMUA-D1YXaTAhSoU9y5CQL-Ect-gNQBvnTdlEvFucffchm3dyXvcnIVb2ZyvHVDrJ9eoaPeDRVeP9QTdHP5-fv5VbP--mV1vlw3ndBialxPnGeKE2mUD-Ap1Q6Mp0SzHgLzWmvJuQ_EMSWF8EAD6QLVgsi2457yE_TxwB33fgehgzQVN9ixzK7Lnc0u2v8nKW7tJt9aRShXWs2AdwdAV-J8a7IpF2cpMZJZJYwUs-L0YUXJv_fzQ-wu1g6GwSXI-2oZYVwzY8y9m_ePsFxrgf7JCCX2PkG7Wq7s3wQtNbP87b_mn8SPkfE_x5aYBg</recordid><startdate>20180701</startdate><enddate>20180701</enddate><creator>Olsen, Ingar</creator><creator>Nichols, Frank C</creator><general>American Society for Microbiology</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>3HK</scope><scope>5PM</scope></search><sort><creationdate>20180701</creationdate><title>Are Sphingolipids and Serine Dipeptide Lipids Underestimated Virulence Factors of Porphyromonas gingivalis?</title><author>Olsen, Ingar ; Nichols, Frank C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-af0ab2630586bdeb117ae8b1072fed2b777533bd0a26544be1d0cd174059c3b13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Alveolar Bone Loss - etiology</topic><topic>Ceramides - chemistry</topic><topic>Ceramides - physiology</topic><topic>Chronic Periodontitis - etiology</topic><topic>Humans</topic><topic>Lipopeptides - chemistry</topic><topic>Lipopeptides - physiology</topic><topic>Minireview</topic><topic>Osteoclasts - physiology</topic><topic>Phosphorylation</topic><topic>Porphyromonas gingivalis - pathogenicity</topic><topic>Toll-Like Receptor 2 - physiology</topic><topic>Virulence Factors - chemistry</topic><topic>Virulence Factors - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Olsen, Ingar</creatorcontrib><creatorcontrib>Nichols, Frank C</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>NORA - Norwegian Open Research Archives</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Infection and immunity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Olsen, Ingar</au><au>Nichols, Frank C</au><au>Maurelli, Anthony T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Are Sphingolipids and Serine Dipeptide Lipids Underestimated Virulence Factors of Porphyromonas gingivalis?</atitle><jtitle>Infection and immunity</jtitle><addtitle>Infect Immun</addtitle><date>2018-07-01</date><risdate>2018</risdate><volume>86</volume><issue>7</issue><issn>0019-9567</issn><eissn>1098-5522</eissn><abstract>The keystone periodontal pathogen produces phosphorylated dihydroceramide lipids (sphingolipids) such as phosphoethanolamine dihydroceramide (PE DHC) and phosphoglycerol dihydroceramide (PG DHC) lipids. Phosphorylated DHCs (PDHCs) from can affect a number of mammalian cellular functions, such as potentiation of prostaglandin secretion from gingival fibroblasts, promotion of RANKL-induced osteoclastogenesis, promotion of apoptosis, and enhancement of autoimmunity. In , these lipids affect anchoring of surface polysaccharides, resistance to oxidative stress, and presentation of surface polysaccharides (anionic polysaccharides and K-antigen capsule). In addition to phosphorylated dihydroceramide lipids, serine dipeptide lipids of are implicated in alveolar bone loss in chronic periodontitis through interference with osteoblast differentiation and function and promotion of osteoclast activity. As a prerequisite for designation as bacterial virulence factors, bacterial sphingolipids and serine dipeptide lipids are recovered in gingival/periodontal tissues, tooth calculus, human blood, vascular tissues, and brain. In addition to , other bacteria of the genera , , , , and produce sphingolipids and serine dipeptide lipids. The contribution of PDHCs and serine dipeptide lipids to the pathogenesis of periodontal and extraoral diseases may be an underappreciated area in microbe-host interaction and should be more intensively investigated.</abstract><cop>United States</cop><pub>American Society for Microbiology</pub><pmid>29632248</pmid><doi>10.1128/iai.00035-18</doi><oa>free_for_read</oa></addata></record>
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source MEDLINE; NORA - Norwegian Open Research Archives; American Society for Microbiology Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central
subjects Alveolar Bone Loss - etiology
Ceramides - chemistry
Ceramides - physiology
Chronic Periodontitis - etiology
Humans
Lipopeptides - chemistry
Lipopeptides - physiology
Minireview
Osteoclasts - physiology
Phosphorylation
Porphyromonas gingivalis - pathogenicity
Toll-Like Receptor 2 - physiology
Virulence Factors - chemistry
Virulence Factors - physiology
title Are Sphingolipids and Serine Dipeptide Lipids Underestimated Virulence Factors of Porphyromonas gingivalis?
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